Phenytoin has been reported to cause an elevation of plasma phenobarbital in epileptic patients. Phenytoin has been shown in patients to 1) stimulate the metabolism of primidone to phenobarbital and 2) inhibit the hydroxylation of phenobarbital. The concomitant rise in phenobarbital levels can cause sedation in epileptic patients. The use of an in vitro system of hepatic microsomes can be of benefit in elucidating the mechanism of this drug-drug interaction. Microsomes will be obtained from adult male phenobarbital-treated Holtzman rats. The rate of phenobarbital production from primidone and the hydroxylation of phenobarbital will be followed at 37 C in NADPH and NADP system. The Michaelis constant (Km) Maximal Velocity (Vmax) will be determined for the conversion of primidone to phenobarbital and for the conversion of phenobarbital to hydroxy-phenobarbital. The inhibition constant (Ki) will be determined for phenytoin in this system.